Early phase microvascular interactions in rat jejunum between nitric oxide and vasopressin following indomethacin administration

Ferenc Lászloa, Brendan Jr Whittle

Research output: Contribution to journalArticle


The involvement of endogenous vasopressin in the actions of indomethacin following the concurrent administration of the nitric oxide (NO) synthase inhibitor, NG-nitro-l-arginine methyl ester (l-NAME), on acute intestinal microvascular permeability has been investigated in the rat. Administration of indomethacin (10mg/kg, s.c.) or L-NAME (10mg/kg, s.c.) alone did not affect jejunal and ileal vascular permeability after 1 h, as determined by the leakage of radiolabelled serum albumin. In contrast, when indomethacin (10mg/kg, s.c.) was injected concurrently with L-NAME (2-10mg/kg, s.c), significant dose-dependent plasma leakage occurred in the jejunum. Pretreatment with l-arginine (300 mg/kg s.c.) 15 min prior to l-NAME prevented these changes in microvascular permeability. Moreover, pretreatment with the vasopressin pressor-receptor antagonist, d(CH2)5Tyr(Me)AVP (0.01-0.2m̈g/kg, s.c.) dose-dependently attenuated such damage. These findings suggest that following indomethacin administration, the early inhibition of NO synthase leads to acute microvascular injury involving vasopressin in the rat jejunum. This suggests a protective role of NO, formed by constitutive NO synthase, counteracting effectively the deleterious actions of endogenous vasopressin.

Original languageEnglish
Pages (from-to)S262-S265
JournalJournal of Gastroenterology and Hepatology (Australia)
Issue numberSUPPL.1
Publication statusPublished - Jan 1 1998



  • Indomethacin
  • Intestinal inflammation
  • Nitric oxide
  • Plasma leakage
  • Vasopressin
  • Vasopressin receptor antagonist

ASJC Scopus subject areas

  • Hepatology
  • Gastroenterology

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